Schneider A
Frauenklinik, University of Ulm, Germany.
Genitourin Med. 1993 Jun;69(3):165-73. doi: 10.1136/sti.69.3.165.
Clinical, subclinical, and latent human papillomavirus (HPV) infections are distinguished from HPV-associated neoplasia. Besides HPV additional cofactors are necessary to transform HPV infected tissue to intraepithelial or invasive neoplasia. Risk factors for the presence of HPV are high number of sexual partners, early cohabitarche, young age at first delivery, suppression and alteration of immune status, young age and hormonal influences. While the fact of a high number of sexual partners exclusively increases the risk of HPV infection, it is not known whether the other factors lead to either an increased risk for HPV infection and/or to HPV-associated neoplasia. Subclinical and latent genital HPV infections are highly prevalent. The prevalence rate depends on the sensitivity of the HPV detection system used, on age and sexual activity of the population screened, and on the number of subsequent examinations performed for each subject. Sexual transmission is the main pathway for genital HPV's, however, vertical, peripartal, and oral transmission are also possible. Seroreactivity against genital HPV may be due to an active infection or the result of contact with HPV earlier in life. Antibodies against the HPV 16 E7 protein indicate an increased risk for cervical cancer. Compared with humoral response cellular immune response is probably more important for regression of genital HPV infection: impaired cellular response is characterized by depletion of T helper/inducer cells and/or Langerhans cells and impaired function of natural killer cells and/or the infected keratinocyte. In condylomata replication and transcription of viral nucleic acids and antigen production coincide with cellular differentiation. However, the interaction between HPV and the keratinocyte on a molecular level in subclinical and latent disease is not well understood. Regression or persistence of subclinical and latent genital HPV infections as observed in longitudinal investigations show a constant come-and-go of HPV presence. Subclinical or latent cervical infections with high-risk HPV types (such as HPV 16 and 18) have an increased risk for the development of HPV-associated neoplasia.
临床、亚临床和潜伏性人乳头瘤病毒（HPV）感染与HPV相关肿瘤有所不同。除了HPV之外，还需要其他辅助因素才能将HPV感染的组织转变为上皮内瘤变或浸润性肿瘤。HPV存在的危险因素包括性伴侣数量多、初次同居年龄早、首次分娩时年龄小、免疫状态受到抑制和改变、年龄小以及激素影响。虽然性伴侣数量多这一事实仅会增加HPV感染的风险，但尚不清楚其他因素是否会导致HPV感染风险增加和/或HPV相关肿瘤的风险增加。亚临床和潜伏性生殖器HPV感染非常普遍。患病率取决于所使用的HPV检测系统的敏感性、所筛查人群的年龄和性活动情况以及对每个受试者进行后续检查的次数。性传播是生殖器HPV的主要传播途径，不过，垂直传播、围产期传播和口传播也是可能的。针对生殖器HPV的血清反应性可能是由于活跃感染或早年接触HPV的结果。针对HPV 16 E7蛋白的抗体表明患宫颈癌的风险增加。与体液反应相比，细胞免疫反应可能对生殖器HPV感染的消退更为重要：细胞反应受损的特征是辅助性/诱导性T细胞和/或朗格汉斯细胞耗竭以及自然杀伤细胞和/或被感染角质形成细胞的功能受损。在尖锐湿疣中，病毒核酸的复制和转录以及抗原产生与细胞分化同时发生。然而，在亚临床和潜伏性疾病中，HPV与角质形成细胞在分子水平上的相互作用尚不清楚。纵向研究中观察到的亚临床和潜伏性生殖器HPV感染的消退或持续表明HPV的存在呈持续的时有时无状态。亚临床或潜伏性宫颈高危HPV类型（如HPV 16和18）感染会增加发生HPV相关肿瘤的风险。
